We [33] and others [34,35,36] have previously used various mouse models of DMD/BMD (mdx—dystrophin-deficient, classical dystrophinopathy mouse model [37]; mdx5cv—mdx strain with a different point mutation [38]; mdx-utr—both dystrophin- and utrophin-deficient, more severe disease phenotype [39,40]) to study the properties of Na+ channels in dystrophic cardiomyocytes. Here, DMD is linked to Duchenne muscular dystrophy.